Hemostasis and Endothelial Function

Abstract

A prothrombotic state (i.e., “thickened blood”s), which can include hemostatic and endothelial changes, contributes to atherosclerosis progression as well as to atherosclerotic plaque rupturing, ultimately leading to myocardial infarction. Acute psychosocial stress elicits a significant increase in several prothrombotic factors. It is important to note that thickening of the blood, as mediated by acute sympathetic nervous system activation, is biologically reasonable and does not usually impose harm to a healthy organism. Rather it protected our ancestors from overt bleeding when injured in fight-flight. However, several factors modulate the magnitude of the acute prothrombotic stress responses that are clearly exaggerated in individuals with an impaired endothelium and cardiovascular diseases. The prothrombotic state associated with chronic psychosocial stress, such as job strain and providing care for a spouse with dementia, might contribute to increased cardiovascular risk even in previously healthy individuals. Particularly autonomic dysfunction and alteration in the hypothalamic pituitary adrenal axis might mediate perturbed hemostatic and endothelial function under chronic stress and negative affect, e.g., depression, hostility, and anxiety.